AIM: To investigate the effect of taurine on the expression of glucose transporter 1 (GLUT1) and transporter 3(GLUT3) in rat brain with diffused brain injury(DBI). METHODS: Sixty-four male Sprague-Dawley rats were randomly divided into 4 groups: sham-operated group,DBI group,low-dose taurine group(200 mg/kg,ig) and high-dose taurine group(300 mg/kg,ig).After fed with the corresponding drugs for 7 days,the animal model of DBI was made,and the rats were executed 24 h after DBI.The expression of GLUT1 and GLUT3 in the brain was detected by the methods of immunohistochemistry and Western blotting.The pathomorphological changes of the cerebral cortex were observed under electron microscope.RESULTS: The expression of GLUT1 was detected in capillary vascular endothelial cells in each group,and cytoplasm-positive cells or the cells with buffy membrane were observed.No significant difference of the GLUT1 expression in brain tissues between DBI group and sham-operated group was detected.Compared with DBI group,the expression of GLUT1 in the brain tissues were significantly increased in low-and high-dose taurine groups(P0.01).The expression of GLUT1 in the brain tissues in low-dose taurine group were significantly higher than that in high-dose taurine group(P0.05).The positive staining of GLUT3 only appeared in the periphery of the third ventricle in each group in the cells with buffy membrane or positive cytoplasm.The expression of GLUT3 in the brain tissues in DBI group was significantly higher than that in sham-operated group(P0.01).The expression of GLUT3 in the brain tissues in low-and high-dose taurine groups was significantly higher than that in DBI group(P0.01).Compared with low dose taurine group,the expression of GLUT3 in the brain tissues were significantly increased in high-dose taurine group(P0.01).The pathological damage of cerebral cortex in low-dose taurine group was obviously alleviated.CONCLUSION: Taurine may take part in the neuroprotective mechanisms in DBI by increasing the expression of GLUT1 and GLUT3 at protein level to maintain the energy supply in brain tissues.